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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Test Results
Assessment
The presentation of a patient with a history of alcohol abuse who is disoriented, agitated,
hallucinating, and perspiring is classic of delirium tremens. Acute confusion and fever are
suggestive of meningitis and this can be excluded with a lumbar puncture if the diagnosis is not
certain. The acute change in mental status may also be due to a CNS bleed precipitated by
falling. The more mild alcohol withdrawal syndrome is often referred to as “impending DTs.”
The symptoms can generally be managed with oral benzodiazepines. Alcoholic hallucinosis
presents with visual hallucinations (as opposed to auditory hallucinations) and is generally
Electrolytes
Blood alcohol level
Serum magnesium level
Arterial blood gases
CT scan of head
Lumbar puncture
Toxicology screen
Blood cultures
Urinalysis
Sodium 146 mEq/L; chloride 108 mEq/L; BUN 30 mg/dL; creatinine 1.3 U/L
Blood alcohol 0.00 mg/dL
Serum magnesium 0.8 mg/dL (1.8–3.0 normal)
pH 7.46; pCO
2
32 mm Hg; pO
2
84 mm Hg; HCO
3
24 mm Hg; O
2
saturation 96%
CT scan: no evidence of bleeding or trauma
Lumbar puncture: normal WBC, protein normal, glucose normal
Toxicology negative
Blood cultures: no growth
Urinalysis: no WBCs
231
distinguished from acute schizophrenia by the history of prolonged alcohol use followed by a
period of cessation. The treatment is the same as for delirium tremens.
Further Management Plan Results
No infiltrates
Normal
Normal
CCS NOTE
There is no specific test to diagnose alcohol withdrawal. It is a diagnosis of exclusion,
along with a history of high-volume alcohol consumption.
Treatment Plan
Chest x-ray
1.
Vitamin B12 level
2.
Liver function tests
3.
IV chlordiazepoxide 50–100 mg every 4–6 hrs and as needed (could also choose other
agents, e.g., diazepam, lorazepam, or phenobarbital)
IV thiamine and folic acid
Start IV fluids D5NS and adjust depending on patient’s hemodynamic status
Magnesium sulfate replacement
Clonidine can also be helpful to suppress some of the cardiovascular hyperexcitability
Atenolol can be used as an adjunct to the benzodiazepines for the tachycardia
Admission to general floor if the withdrawal is mild or to the ICU if patient has severe
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CCS NOTE
In patients with a clear presentation of alcohol withdrawal and delirium tremens,
medical therapy such as lorazepam and chlordiazepoxide should be ordered before the
results of the tests are known.
Discussion
Abstinence or withdrawal syndrome refers to a constellation of symptoms that develop only
after a period of relative or absolute abstinence from alcohol. The syndrome may develop in
the periodic drinker, as well as the chronic drinker.
Delirium tremens is the most serious form of the syndrome and an acute medical emergency. It
should not be confused with the more mild signs and symptoms of alcohol withdrawal such as
tremulousness. Seizures may develop, which may be fatal. If left untreated, mortality rate is up
to 15%. It is characterized by:
symptoms (e.g., seizures)
Delusions
Generalized seizures
Profound confusion
Visual hallucinations
Tremor
Agitation
Increased activity of ANS, e.g., dilated pupils, fever, tachycardia, perspiration
233
Symptoms generally develop 9–12 hrs after the last drink, peaking at 48–72 hrs. Laboratory
hallmarks include hypomagnesemia, decreased arterial pH, and decreased pO
2
. There are also
derangements in the serum electrolytes that are most often related to dehydration.
The initial evaluation should be thorough, paying special attention to possible associated
injuries the patient may have sustained due to the state of agitation and altered mental status.
Patients frequently fall before they arrive for medical attention, are in a poor state of health,
and often suffer from malnutrition.
Special attention should be given to the issue of glucose administration in the IV fluids. The
alcoholic patient generally lives on a diet high in carbohydrates (alcohol) and low in thiamine,
and tends to have no vitamin B reserves. The administration of glucose will consume the
patient’s last stores of thiamine and may precipitate Wernicke’s syndrome. There is no
definitive proof, however, that giving the thiamine just before or after the dextrose really makes
any difference because they are given so closely together.
The goal of therapy is to provide medication that (a) is cross-tolerant for alcohol, and (b) will
blunt the patient’s state of agitation and thereby prevent exhaustion. This is best achieved with
benzodiazepines or chlordiazepoxide; however, the specific agent used is not as important as
using a sufficiently high amount of the medication.
Basic Science Correlate
Phenytoin is not useful for withdrawal-related seizures.
Haldoperidol should be avoided because it can lower the seizure threshold.
If the patient has liver failure, lorazepam and oxazepam are the only safe agents.
If the patient is refractory to benzodiazepines, barbiturates or propofol can be effective.
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Benzodiazepines activate GABA receptors, which increase the chloride current in
neurons of the CNS. This leads to hyperpolarization of neurons and inhibits firing of
action potentials (inhibitory potentials).
Thiamine deficiency can lead to Wernicke–Korsakoff syndrome. Wernicke is the triad of
confusion, ataxia, and ophthalmoplegia (weakness or paralysis (-plegia) of ≥1 extraocular
muscles which are responsible for eye movements). It is reversible with thiamine treatment.
Korsakoff is amnesia with confabulation. It is irreversible.
Thiamine deficiency may also lead to wet beri beri, which is high cardiac output failure. This,
like other causes of high cardiac output failure (chronic anemia, arteriovenous fistula, Paget’s
disease of bone, hyperthyroidism), is due to intense vasodilation of the peripheral arterioles
because of the loss of ability to vasoconstrict secondary to low ATP levels. This leads to
increases in cardiac output because of the decrease in resistance (low afterload) and an
increase in venous return. The chronically elevated venous return overworks the heart and
leads to eccentric hypertrophy (dilated cardiomyopathy). The patient presents with edema, and
shortness of breath due to pulmonary edema
.
Basic Science Correlate
Patents with thiamine deficiency have decreased activity of 3 important enzymes:
Pyruvate dehydrogenase
α-ketoglutarate dehydrogenase
Transketolase
235
Thiamine is a co-factor for the enzymes above. All of these enzymes are necessary for normal
production of ATP and patients with thiamine deficiency have decreased utilization of glucose
because they are not able to produce ATP.
Pyruvate dehydrogenase complex catalyzes the following reaction:
Pyruvate + NAD + CoA → acetyl-CoA + CO
2
+ NADH
The pyruvate dehydrogenase complex requires 5 cofactors:
The end product of the pyruvate dehydrogenase complex is acetyl-CoA, which then enters the
citric acid cycle. Impairment of the complex can cause tissues (e.g., brain and heart) to be
affected by low ATP.
Final Diagnosis
Alcohol withdrawal with delirium tremens
Pyrophosphate (B1, thiamine; TPP)
1.
FAD (B2, riboflavin)
2.
NAD (B3, niacin)
3.
CoA (B5, pantothenate)
4.
Lipoic acid
5.
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Case 2
Chief Complaint
“I can’t walk right.”
History and Physical Examination
A 19-year-old white man who was playing rugby 6 hrs ago comes to the emergency
department complaining of a severe headache for the last 2 hrs. While playing, he
sustained head trauma and had a brief period of loss of consciousness from which he
awoke and was his normal self. He then started to complain of nausea, vomiting, and
weakness of the right side, as well as an inability to walk. He has no other medical
problems.
Vital signs are T 37.8° C (100° F), BP 120/80 mm Hg, pulse 88/min, and respirations
18/min. Neurologic examination shows a small laceration of the left temporal region. His
right eye is normal, and his left eye is dilated. There is a right hemiplegia. The remainder
of the physical examination is unremarkable.
CCS NOTE
All patients with head trauma and a loss of consciousness should undergo a head CT
scan without contrast, no matter how brief the loss of consciousness.
237
Differential Diagnosis
Initial Management
Initial Management Plan Results
Convex hyperdensity between the brain and
skull, consistent with an acute epidural
hematoma. A midline shift to the right is seen.
Setting: emergency department
Assessment
Rapidly evolving and often lethal, acute epidural hematomas are formed by laceration of a
dural vessel, which produces a clot between the skull and the dura. Hemorrhage originates
most often from a branch of the middle meningeal artery that has been lacerated by a fracture.
In 90% of adult patients with an epidural hematoma, skull fracture is demonstrated by x-ray or
at surgery or autopsy. The classic history is a brief loss of consciousness from which the
patient awakens and is completely well; then the clot forms, compressing the brain surface and
increasing the overall intracranial pressure. The increased pressure results in headache,
vomiting, and weakness of contralateral limbs. The temporal lobe is displaced, compressing
the brainstem and the adjacent ipsilateral occulomotor nerve.
Subdural hematoma
1.
Concussion
2.
Epidural hematoma
3.
Contusion
4.
Subarachnoid hemorrhage
5.
CT scan of head, without contrast
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CCS NOTE
Although not repeatedly mentioned in every one of these cases, every patient scheduled
to have surgery should have a CBC to assess the platelet count and a prothrombin time
to assess the risk of bleeding during the procedure.
Treatment plan
CCS NOTE
Stress ulcer prophylaxis is given for any patient who has had head trauma, burns, or
intubation.
Discussion
In acute epidural hematoma, careful observation of the level of consciousness and the
neurologic status is imperative if an epidural hematoma is considered. Earliest possible
evacuation of the hematoma before transtentorial herniation can occur is essential for a
Intubation and hyperventilation to a pCO
2
of 25-30 mm Hg1.
IV mannitol use2.
Neurosurgical evaluation for surgical evacuation of the hematoma3.
Maintain systolic BP greater than 100 mm Hg4.
Stress ulcer prophylaxis with proton pump inhibitors, H
2
blockers, or sucralfate5.
Admission to the intensive care unit6.
239
favorable outcome. Studies have shown that once signs of herniation are present,
approximately 73% of patients who were decerebrate before surgery died. However, only 1%
of patients died before surgery when they presented conscious, with no signs of herniation
prior to surgery. The 2 essential components of a successful procedure are (a) removing the
clot to relieve brain compression, and (b) securing the source of bleeding to prevent
recurrence. As the clot is removed, hemostasis is achieved by electrocoagulation and ligation
of the main trunks of the middle meningeal vessels as they appear on the dura.
The acute management of increased intracranial pressure involves hyperventilation and
mannitol injection. Hyperventilation lowers the pCO
2
of the arterial blood, and the cerebral
vessels will therefore constrict. This will reduce intracranial pressure. Mannitol is an osmotic
diuretic that also acutely decreases intravascular volume.
Steroids are of no benefit in intracranial bleeding. Their best indication is to decrease swelling
around brain tumors, such as neoplasms and infection, which lead to increased intracranial
pressure from edema.
CCS NOTE
For every CCS case, make sure to address location. Don’t leave your patient in the
emergency department after the initial management is complete. This patient will be
transferred to the surgical ICU or directly to the OR.
Final Diagnosis
Epidural hematoma, acute
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